About: The ER stress sensor IRE1 and MAP kinase ERK modulate autophagy induction in cells infected with coronavirus infectious bronchitis virus

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About: The ER stress sensor IRE1 and MAP kinase ERK modulate autophagy induction in cells infected with coronavirus infectious bronchitis virus Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The ER stress sensor IRE1 and MAP kinase ERK modulate autophagy induction in cells infected with coronavirus infectious bronchitis virus
Creator	Fung, Ding Liu, To, Sing
topic	covid:232aa59a63dce6c8f0aa823a43534d1267577c94#this
Source	Elsevier; Medline; PMC
abstract	Abstract Coronavirus infection induces the generation of autophagosomes, and certain host proteins regulating cellular autophagy are hijacked by some coronaviruses to facilitate the formation of double membrane vesicles. However, mechanisms underlying coronavirus-induced autophagy remain largely unknown. In this study, we demonstrate that autophagosome formation and apparent autophagic flux are induced in cells infected with infectious bronchitis virus (IBV) – a gammacoronavirus. Notably, IBV-induced autophagy was dependent on autophagy related 5 (ATG5) but not beclin1 (BECN1), although both are essential proteins in the canonical autophagy pathway. Moreover, the ER stress sensor inositol requiring enzyme 1 (IRE1), but not its substrate X-box protein 1 (XBP1), was also essential for the induction of autophagy during IBV infection. Finally, the anti-apoptotic extracellular signal-regulated kinase 1/2 (ERK1/2) also contributed to IBV-induced autophagy. Our findings add new knowledge to the regulatory mechanisms governing coronavirus-induced autophagy, highlighting an extensive cross-talk among cellular signaling pathways during coronavirus infection.
has issue date	2019-07-31(xsd:dateTime)
bibo:doi	10.1016/j.virol.2019.05.002
bibo:pmid	31082732
has license	els-covid
sha1sum (hex)	232aa59a63dce6c8f0aa823a43534d1267577c94
schema:url	https://doi.org/10.1016/j.virol.2019.05.002
resource representing a document's title	The ER stress sensor IRE1 and MAP kinase ERK modulate autophagy induction in cells infected with coronavirus infectious bronchitis virus
has PubMed Central identifier	PMC7112053
has PubMed identifier	31082732
schema:publication	Virology
resource representing a document's body	covid:232aa59a63dce6c8f0aa823a43534d1267577c94#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/232aa59a63dce6c8f0aa823a43534d1267577c94
is schema:about of	named entity 'INFECTED' named entity 'AUTOPHAGY' named entity 'double' named entity 'remain' named entity 'highlighting' named entity 'autophagy' named entity 'Coronavirus' named entity 'sensor' named entity 'ER STRESS SENSOR' named entity 'AUTOPHAGY' named entity 'CORONAVIRUS' named entity 'CELLS' named entity 'INFECTIOUS BRONCHITIS VIRUS' named entity 'SIGNALING PATHWAYS' named entity 'PROTEIN ' named entity 'ER STRESS SENSOR' named entity 'CORONAVIRUS' named entity 'REGULATING' named entity 'CELLULAR' named entity 'EXTENSIVE' named entity 'PROTEIN KINASE A' named entity 'UNKNOWN' named entity 'INDUCTION' named entity 'GAMMACORONAVIRUS' named entity 'EXTRACELLULAR SIGNAL-REGULATED KINASE 1' named entity 'VESICLES' named entity 'MECHANISMS' named entity 'ER STRESS' named entity 'CORONAVIRUS INFECTION' named entity 'MITOGEN-ACTIVATED PROTEIN KINASE' named entity 'BECLIN1' named entity 'MODULATE' named entity 'ERK' named entity 'AUTOPHAGY RELATED 5' named entity 'UNFOLDED PROTEIN RESPONSE' named entity 'APPARENT' named entity 'IRE1' named entity 'MAP KINASE' named entity 'MEMBRANE' named entity 'UNDERLYING' named entity 'INDUCED' named entity 'INFECTIOUS BRONCHITIS VIRUS' named entity 'OUR' named entity 'HOST' named entity 'FORMATION' named entity 'INDUCTION' named entity 'ITS' named entity 'DEPENDENT' named entity 'REGULATORY' named entity 'ENZYME' named entity 'ADD' named entity 'NEW KNOWLEDGE' named entity 'CERTAIN' named entity 'FLUX' named entity '29A' named entity 'CROSS-TALK' named entity 'INFECTED' named entity 'STUDY' named entity 'GENERATION' named entity 'SUBSTRATE' named entity 'INFECTION' named entity 'S T' named entity 'AUTOPHAGOSOME FORMATION' named entity 'ANTIAPOPTOTIC' named entity 'CELLS' named entity 'BUT' named entity 'AUTOPHAGOSOMES' named entity 'CORONAVIRUSES' named entity 'FINDINGS' named entity 'HIGHLIGHTING' named entity 'DOUBLE' named entity 'PROTEINS' named entity 'AUTOPHAGY PATHWAY' named entity 'LARGELY' named entity 'ESSENTIAL' named entity 'INOSITOL' named entity 'Xbox'

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